ArticleThe Journal of cell biology2003
Intact satellite cells lead to remarkable protection against Smn gene defect in differentiated skeletal muscle.
Article in The Journal of cell biology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
60 citing papers in PubMed, 95 citations in OpenAlex.
- Targeted knockdown of Smn in muscle stem cells induces non-cell autonomous loss of motor neurons.Brain : a journal of neurology · 2026Article
- Survival Motor Neuron Protein Requirement-Supply Mismatch in Spinal Muscular Atrophy: A Conceptual Framework.Advances in therapy · 2026Review
- Txnrd2 loss in skeletal muscle causes muscle atrophy and drives leanness and obesity resistance.Redox biology · 2026Article
- RNA biomarkers in spinal muscular atrophy: enhancing pathogenesis understanding and guiding precision medicine.Cellular and molecular life sciences : CMLS · 2026Review
- SMN depletion impairs skeletal muscle formation and maturation in a mouse model of SMA.Human molecular genetics · 2025Article
- Muscle: an independent contributor to the neuromuscular spinal muscular atrophy disease phenotype.JCI insight · 2023Review
- Innovating spinal muscular atrophy models in the therapeutic era.Disease models & mechanisms · 2023Article
- SMN promotes mitochondrial metabolic maturation during myogenesis by regulating the MYOD-miRNA axis.Life science alliance · 2023Article
- A link between agrin signalling and CaScientific reports · 2022Article
- Therapy development for spinal muscular atrophy: perspectives for muscular dystrophies and neurodegenerative disorders.Neurological research and practice · 2022Review
- Genomic Variability in the Survival Motor Neuron Genes (International journal of molecular sciences · 2021Review
- The relationship between muscle stem cells and motor neurons.Cellular and molecular life sciences : CMLS · 2021Review
- Dysregulation of Muscle-Specific MicroRNAs as Common Pathogenic Feature Associated with Muscle Atrophy in ALS, SMA and SBMA: Evidence from Animal Models and Human Patients.International journal of molecular sciences · 2021Article
- Spinal muscular atrophy: Broad disease spectrum and sex-specific phenotypes.Biochimica et biophysica acta. Molecular basis of disease · 2021Review
- Exclusive vital labeling of myonuclei for studying myonuclear arrangement in mouse skeletal muscle tissue.Skeletal muscle · 2020Article
- mTORC2 affects the maintenance of the muscle stem cell pool.Skeletal muscle · 2019Article
- Lack of muscle mTOR kinase activity causes early onset myopathy and compromises whole-body homeostasis.Journal of cachexia, sarcopenia and muscle · 2019Article
- Low-Intensity Running and High-Intensity Swimming Exercises Differentially Improve Energy Metabolism in Mice With Mild Spinal Muscular Atrophy.Frontiers in physiology · 2019Article
- Impaired myogenic development, differentiation and function in hESC-derived SMA myoblasts and myotubes.PloS one · 2018Article
- First Characterization of Human Amniotic Fluid Stem Cell Extracellular Vesicles as a Powerful Paracrine Tool Endowed with Regenerative Potential.Stem cells translational medicine · 2017Article
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Deletion of murine Smn exon 7, the most frequent mutation found in spinal muscular atrophy, has been directed to either both satellite cells, the muscle progenitor cells and fused myotubes, or fused myotubes only. When satellite cells were mutated, mutant mice develop severe myopathic process, progressive motor paralysis, and early death at 1 mo of age (severe mutant). Impaired muscle regeneration of severe mutants correlated with defect of myogenic precursor cells both in vitro and in vivo. In contrast, when satellite cells remained intact, mutant mice develop similar myopathic process but exhibit mild phenotype with median survival of 8 mo and motor performance similar to that of controls (mild mutant). High proportion of regenerating myofibers expressing SMN was observed in mild mutants compensating for progressive loss of mature myofibers within the first 6 mo of age. Then, in spite of normal contractile properties of myofibers, mild mutants develop reduction of muscle force and mass. Progressive decline of muscle regeneration process was no more able to counterbalance muscle degeneration leading to dramatic loss of myofibers. These data indicate that intact satellite cells remarkably improve the survival and motor performance of mutant mice suffering from chronic myopathy, and suggest a limited potential of satellite cells to regenerate skeletal muscle.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.